Protein / target

Bcl-2-like protein 1

Encoded byBCL2L1Q07817Homo sapiensSwiss-Prot

UniProt: Q07817 Ensembl: ENSG00000171552 HGNC: HGNC:992 NCBI Gene: 598

Clinically validated

Therapeutic maturity

Approved medicines

Open Targets target-level

Clinical trials

Small-molecule tractable

Druggability

Advanced Clinical

Protein at a glance

Biological role

Identical protein binding

Strongest disease association

Neurodegenerative Diseases

Via encoding gene BCL2L1 · Pathway evidence · score 0.53

Therapeutic position

Established drug target

Small molecules

Derived from structured UniProt, Open Targets and literature data on this page.

Protein profile

UniProt 2026_02

Canonical identity and biological annotation from UniProt.

Function overview

Potent inhibitor of cell death.

View complete UniProt function annotation

Potent inhibitor of cell death. Inhibits activation of caspases. Appears to regulate cell death by blocking the voltage-dependent anion channel (VDAC) by binding to it and preventing the release of the caspase activator, CYC1, from the mitochondrial membrane. Also acts as a regulator of G2 checkpoint and progression to cytokinesis during mitosis

Subcellular location

Mitochondrion inner membraneMitochondrion outer membraneMitochondrion matrixCytoplasmic vesicle, secretory vesicle, synaptic vesicle membraneCytoplasm, cytosolCytoplasm, cytoskeleton, microtubule organizing center, centrosomeNucleus membrane

Domains and Gene Ontology detail (38)

Gene Ontology

CBcl-2 family protein complex
Ccentrosome
Ccytoplasm
Ccytosol
Cendoplasmic reticulum
Cmitochondrial inner membrane
Cmitochondrial matrix
Cmitochondrial outer membrane
Cmitochondrion
Cnuclear membrane
Csynaptic vesicle membrane
FBH3 domain binding

233 aa · 26 kDa · 3 isoforms

Biological roles

Reactome v97

What this protein does, drawn together from its UniProt function, Gene Ontology terms and Reactome pathways.

Immune signallingUniProt · GO · ReactomeApoptosis & cell deathUniProt · GO · Reactome

View supporting evidence

Immune signalling

·Potent inhibitor of cell death. Inhibits activation of caspases. Appears to regulate cel…
·regulation of cytokinesis
·response to cytokine
·Interleukin-4 and Interleukin-13 signaling

Apoptosis & cell death

·Potent inhibitor of cell death. Inhibits activation of caspases. Appears to regulate cel…
·negative regulation of apoptotic process
·positive regulation of apoptotic process
·SARS-CoV-1-mediated effects on programmed cell death

View underlying pathways (7)

BH3-only proteins associate with and inactivate anti-apoptotic BCL-2 members

Interleukin-4 and Interleukin-13 signaling

The NLRP1 inflammasome

RAS processing

SARS-CoV-1-mediated effects on programmed cell death

STAT5 activation downstream of FLT3 ITD mutants

NFE2L2 regulating tumorigenic genes

Concepts derived from UniProt GO Reactome — each badge above shows which sources supported that role.

Interaction neighbourhood

STRING v12.0

Proteins with the strongest functional or physical association. Node size and line weight reflect STRING confidence; hover or select a partner to inspect one association.

10 strongest partners — larger node and heavier line mean higher confidence

Functional and physical associations from STRING v12.0. Only associations with this protein are drawn — partner-to-partner links are not part of this evidence.

Drugs targeting this protein

How approved and investigational drugs engage this protein — mechanism and action type, direct vs complex targeting, and how broadly each acts across other targets. A drug-first view (the section above groups the approved ones disease-first); direct binders with few recorded targets are listed first.

navitoclax

Narrow target profileApprovedInhibitor

Apoptosis regulator Bcl-X inhibitor

Direct interaction with this protein · 1 of 3 recorded protein targets — narrow recorded profile

ChEMBL mechanism, action type, target identity and approved indications. Open Targets clinical status.

Translational evidence

Open Targets 26

Why this target matters therapeutically, strongest evidence first. Disease associations are gene-level (via the gene that encodes this protein) and open into the full confidence synthesis; the development universe, tractability and safety annotations are target-level, from Open Targets.

Strongest disease associations · via encoding gene BCL2L1

Gene-level evidence surfaced through the gene BCL2L1that encodes this protein — not a direct protein–disease relationship. Ranked by Forefront's causal-directness weighting, so genetically- and clinically-evidenced diseases lead over ones that merely share the literature.

Neoplasms

0.55Moderately supported

Clinical evidence dominant · Open Targets 0.41

Myelofibrosis

0.46Limited support

Clinical evidence dominant · Open Targets 0.37

Small Cell Lung Carcinoma

0.43Limited support

Clinical evidence dominant · Open Targets 0.31

Neurodegenerative Diseases

0.35Preliminary

Pathway evidence dominant · Open Targets 0.53 · no direct causal or clinical evidence

Severe Acute Respiratory Syndrome

0.31Preliminary

Pathway evidence dominant · Open Targets 0.46 · no direct causal or clinical evidence

View evidence synthesis (5)

NeoplasmsModerately supported

0.55

agreement 0.40–0.71

Clinical77%Literature23%

Open Targets aggregate 0.41 · 2 independent evidence families

MyelofibrosisLimited support

0.46

agreement 0.30–0.61

Clinical95%Literature5%

Open Targets aggregate 0.37 · 2 independent evidence families

Small Cell Lung CarcinomaLimited support

0.43

agreement 0.28–0.59

Clinical73%Literature27%

Open Targets aggregate 0.31 · 2 independent evidence families

Neurodegenerative DiseasesPreliminary

0.35

agreement 0.18–0.53

Pathway97%Literature3%

Open Targets aggregate 0.53 · 2 independent evidence families · no direct causal or clinical evidence

Severe Acute Respiratory SyndromePreliminary

0.31

agreement 0.13–0.48

Pathway99%Literature1%

Open Targets aggregate 0.46 · 2 independent evidence families · no direct causal or clinical evidence

This ranking differs from Open Targets' own: re-weighting moves genetically-evidenced diseases above more heavily co-mentioned ones. The evidence agreement range shows how closely the independent evidence families agree — it is not a statistical confidence interval, and nothing here is fitted to outcome data. Derived from Open Targets evidence types under Forefront weighting; the per-type scores above show the calculation.

Show all associations

Neurodegenerative Diseases0.53

Severe Acute Respiratory Syndrome0.46

Neoplasms0.41

Myelofibrosis0.37

Small Cell Lung Carcinoma0.31

Precursor Cell Lymphoblastic Leukemia-Lymphoma0.14

Leukemia, Myeloid, Acute0.14

Leukemia, Lymphocytic, Chronic, B-Cell0.13

Melanoma0.13

Drug development

3 compounds recorded · 1 approved · 2 in clinical development

Open Targets' development universe — every compound recorded against the target at any stage, not all approved medicines. Distinct from the 1 drug that targets this protein in Forefront's canonical graph: these count different sets and are not a subset relation.

View all recorded compounds (3)

OBATOCLAXPhase 2

NAVITOCLAXApproval

OBATOCLAX MESYLATEPhase 3

Open Targets known-drugs universe. Drug name and highest clinical stage only — the disease relationship is NOT read from this slice (it carries trial-context noise); approved indications come from the canonical graph above.

Tractability

Small molecules — Strong

Advanced Clinical and Structure with Ligand support this modality.

Antibodies — Emerging

Feasibility evidence (uniprot sigp or tmhmm) — no clinical-stage drug of this modality recorded.

Protein degraders — Emerging

Feasibility evidence (literature and uniprot ubiquitination) — no clinical-stage drug of this modality recorded.

View underlying tractability evidence (10)

SM · Advanced ClinicalSM · Structure with LigandSM · High-Quality LigandSM · Druggable FamilyAB · UniProt SigP or TMHMMPR · LiteraturePR · UniProt UbiquitinationPR · Database UbiquitinationPR · Half-life DataPR · Small Molecule Binder

Raw Open Targets tractability assessment buckets, by modality.

Clinical trials

Trials of drugs that target this protein — reached indirectly through those drugs, so a trial listed here studies the drug, not the protein. Ranked by active status, then clinical phase and recency, and spread across the targeting drugs.

Randomized, Open-Label, Phase 3 Study Evaluating Efficacy and Safety of Navitoclax in Combination With Ruxolitinib Versus Best Available Therapy in Subjects With Relapsed/Refractory Myelofibrosis (TRANSFORM-2), Incorporating Extension Arm C - Continued Access for Navitoclax to Roll Over Subjects From Studies M10-166, M16-109, M16-191, and M19-753PHASE3

ACTIVE_NOT_RECRUITING · via navitoclax · NCT04468984

A Phase II Study of Genetically Risk-Stratified Combination of Venetoclax, Ibrutinib and Rituximab (With and Without Navitoclax) in Patients With Relapsed and Refractory Mantle Cell Lymphoma (AIM2)PHASE2

ACTIVE_NOT_RECRUITING · via navitoclax · NCT05864742

RAVEN: A Phase I/II Trial Treating Relapsed Acute Lymphoblastic Leukemia With Venetoclax and NavitoclaxPHASE1/PHASE2

ACTIVE_NOT_RECRUITING · via navitoclax · NCT05192889

A Phase 1b-2 Trial to Assess the Safety and Efficacy of a Venetoclax and Navitoclax Consolidation in High-risk Patients With T- Cell Acute Lymphoblastic Leukemia Prior to Allogeneic Transplantation Followed by Venetoclax and Navitoclax Post-transplant MaintenancePHASE1/PHASE2

NOT_YET_RECRUITING · via navitoclax · NCT05054465

View all trials (20)

An Open Label, Two-Part, Phase Ib/II Study to Investigate the Safety, Pharmacokinetics, Pharmacodynamics, and Clinical Activity of the MEK Inhibitor Trametinib and the BCL2-Family Inhibitor Navitoclax (ABT-263) in Combination in Subjects With KRAS or NRAS Mutation-Positive Advanced Solid TumorsPHASE1/PHASE2

ACTIVE_NOT_RECRUITING · via navitoclax · NCT02079740

Phase I/II Study of Dabrafenib, Trametinib, and Navitoclax in BRAF Mutant Melanoma (Phase I and II) and Other Solid Tumors (Phase I Only)PHASE1/PHASE2